Possible contribution of NO production by iNOS in endotoxin-induced ocular inflammation to the regulation of muscle tone of rat iris sphincter

• Published in: Japanese Journal of Pharmacology 2001, Vol.85 (suppl.2), p.284-284
• Main Authors: Junko Kondo, Chiyo Ito, Michino Furuta, Susumu Ohya, Katsuhiko Muraki, Minoru Watanabe, Yuji Imaizumi
• Format: Article
• Language: Japanese
• ISSN: 0021-5198

When inflammation is elicited by the treatment with endotoxin / lipopolysaccharide (LPS), NO production is dramatically increased following the induction of iNOS. Although NO relaxes smooth muscle via cGMP pathway, ocular inflammation is characterized by miosis. In this study, the relation between NO production by iNOS and iris contractility in ocular inflammation was examined. The induction of iNOS in iris was performed in rats by intravitreal injection of LPS (in vivo), and also by incubation of isolated sphincters with 1 μg/ml LPS (in vitro). The ocular inflammation was confirmed by the increase in leukocytes in aqueous humor. In sphincters isolated from eyes injected with LPS in vivo, iNOSm-RNA was markedly induced and cGMP content was significantly increased, while ACh-induced contraction was not affected by L-NAME or L-arginine. In sphincters treated with LPS in vitro, iNOS-mRNA induction and much larger increase in cGMP than in vivo were demonstrated. Application of L-NAME and L-arginine elicited significant contraction and relaxation, respectively. The increase in cGMP in sphincters by intravitreal injection of LPS was not enough to relax the muscle in spite of the sever inflammation. NO produced by iNOS may not contribute significantly to the regulation of pupil diameter during ocular inflammation.